This proposal is to request support for a pair of concurrent 2007 Keystone meetings entitled Autophagy in Health and Disease and Apoptotic and Non-Apoptotic Cell Death Pathways, which will be held in Monterey, California from April 15-20, 2007. Autophagy is the major pathway that eukaryotic cells use to degrade and recycle cytoplasmic contents during development, tissue homeostasis, and environmental stress. In recent years, there has been an explosion of knowledge about the molecular mechanisms of autophagy and its roles in organelle turnover, cell death regulation, cancer cell biology, innate immunity, aging, and neurodegenerative disorders. This meeting will focus on advances made in these areas, with the goal of understanding the molecular and cellular mechanisms by which autophagy and the deregulation of autophagy contribute to health and disease. In addition, the meeting will focus on how autophagy can be exploited as a therapeutic target in cancer, infectious diseases, aging and neurodegeneration. With regard to the meeting on Apoptotic and Non-Apoptotic Cell Death Pathways, there is an increasing awareness that apoptosis may not be the only cellular mechanism for programmed cell death. The cell death field is on the verge of major breakthroughs in the identification of alternative cellular mechanisms of cell death. Since this will be the first international meeting emphasizing the mechanisms of non-apoptotic cell death, we intend to provide a historical review as well as the current views of apoptotic vs. nonapoptotic cell death mechanisms. The meeting will have two major objectives: document the existence of alternative cellular mechanisms of cell death in normal development, cancer and neurodegenerative diseases; and provide new insights into the molecular mechanisms of non-apoptotic cell death. Holding these 2 meetings jointly will highlight the interplay between autophagy and cell death and foster energetic and critical crosstalk between investigators in these 2 fields. [unreadable] [unreadable] [unreadable]